Deregulated degradation of the cdk inhibitor p27 and malignant transformation
Deregulated degradation of the cdk inhibitor p27 and malignant transformation
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DOI：
10.1016/s1044-579x(02)00098-6
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发表时间：
2003-02-01
影响因子：
14.5
通讯作者：
Pagano, M
中科院分区：
文献类型：
--
作者：
Bloom, J;Pagano, M
p27通过在G 0和G1期间抑制细胞周期蛋白/cdk复合物的活性而作为细胞周期的关键负调节剂。p27的降解是G1/S转换的关键事件，并且通过SCFSkp 2的泛素化和随后的26 S-蛋白酶体的降解而发生。p27的肿瘤抑制功能已在小鼠模型和人类肿瘤研究中得到证实。最近的证据表明，Skp 2，p27泛素化的特异性识别因子，具有致癌特性。本文就p27蛋白水解的调控及其在肿瘤发生中的作用作一综述。(C)2002爱思唯尔科技有限公司版权所有。
p27 acts as a critical negative regulator of the cell cycle by inhibiting the activity of cyclin/cdk complexes during G0 and G1. Degradation of p27 is a critical event for the G1/S transition and occurs through ubiquitination by SCFSkp2 and subsequent degradation by the 26S-proteasome. A tumor suppressing function of p27 has been demonstrated in mouse models and studies of human tumors. More recent evidence suggests that Skp2, the specific recognition factor for p27 ubiquitination, has oncogenic properties. This review will focus on the regulation of p27 proteolysis and its consequences for tumorigenesis. (C) 2002 Elsevier Science Ltd. All rights reserved.